Alterations in body morphology are critical in an organism's ability to adapt to selective pressures. Animals have evolved to display countless innovations and modifications in body form. A longstanding goal in evolutionary and developmental biology is to understand the genetic and molecular bases underlying the evolution of morphology. Anatomical traits are either gained or lost during evolution. The loss of a complex trait is frequent and often requires alternations in a single gene, while a gain of a trait is less frequent and involves multiple loci. Although a growing body of work has addressed the evolution of form, most studies have focused on the role of single genes in the loss of a phenotypic trait. The genetic changes that recruit multiple genes in the gain of a trait have not been examined at the molecular level. Furthermore, while the gain of similar traits in independent lineages is widespread, it is not known if a similar or distinct genetic architecture has evolved to control the development of the trait. I will address these issues in this proposal. Male-specific abdominal pigmentation in Drosophila is a rapidly evolving trait that is governed in D. melanogaster by the action of several well-characterized regulatory and terminal differentiation genes. Recently, it was found that the Abdominal-B Hox protein (Abd-B) directly activates the sex-specific abdominal expression of a pigmentation gene. This poses the hypothesis that other pigmentation genes required for trait development may also be directly regulated by Abd-B, suggesting that several components governing the development of a multigenic trait are controlled by a common genetic regulatory mechanism. In addition, sex-specific abdominal pigmentation has been independently gained in relatively distant Drosophila lineages from D. melanogaster, raising the hypothesis that the same regulatory and terminal differentiation genes, have been independently co-opted in the convergent gain of similar traits. The work proposed here will provide insights into the molecular mechanisms of how a Hox-regulated network [unreadable] [unreadable] [unreadable]